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28 Cards in this Set

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How do you TREAT someone who comes in with diphteria (shown to be toxigenic as well)?
1) DAT - diphtheria antitoxoid (horse serum with Abs against the diphtheria toxin); this will remove DT that has disseminated into the blood stream
2) Antibiotics - C. diphtheriae is susceptible to penicillin; give this to suppress/kill the BACTERIA themselves
3) DTaP - we must vaccinate them because paradoxically, infection does NOT result in immunization with diphtheria
Why do we vaccinate someone anyway who comes in with a diphtheria infection?
Because for some reason unknown, being infected with the bacteria DOES not immunize the host. We must vaccinate them.
What makes the toxins of diphtheria and tetanus such great vaccine candidates?
They are invariable, they haven't change and show no variability for years
Explain the structure & mechanism of the A-B diphtheria toxin first starting outside the cell...
Diphtheria toxin is an A-B toxin that is made uniquely as 1 polypeptide chain at first. When the B unit binds to its surface receptor (EGFR) the peptide gets nicked so that the only thing holding the A and B together still are their disulfide bonds. The toxin is endocytosed into the cell, where in the endosome, once acidification happens, you lose your disulfide bonds and the T unit (not impt) inserts into the endosomal membrane allowing for the A unit to leave into the cytoplasm. Once in the cytoplasm, the A (activity) subunit ADP-ribosylates (from NAD) Elongation Factor 2 (EF-2) at its diphthamide site (a His related residue). This effectively shuts off protein synthesis in that cell.
Characterize Corynebacterium diphteriae
*Gram +
*club shaped
*nonmotile
*forms chains of V or L (chinese lettering)
*nonencapsulated
*non-invase (just sticks to the back of the oral pharynx and sits there pumping out its toxin if its toxigenic)
*shows metachromatic granules (polymetaphosphate) when stained with methylene blue
*resistant to potassium tellurite in that in the presence of potassium tellurite in its growth medium, it will reduce it to black colonies
*non-hemolytic
*very fastidious organism, must grow on special media (Loeffler)
Characterize Lysteria monocytogenes
*gram +
*GROWS AT 4 DEGREES C
*coccobacilus in shape
*motile
*invasive
*facultative intracellular parasite
*reduces tellurite as well like C. diphteria
*weakly hemolytic
*catalase positive
Characterize Bacillus anthracis
*gram +
*sporulates
*bacilli in shape
*capsulated (poly-D-glutamic acid)
*nonmotile (all the other bacilli are motile)
*forms LONG chains
*boxcars with their spores off to one side
Characterize Bacillus cereus
*gram +
*sporulates
*NON-CAPSULATED
*MOTILE!!!
*bacillus in shape
*Forms long chains
What are the two types of enterotoxins Bacillus cereus can make?
1) emetic toxin - rapid onset vomitting - 1-6 horus -reason why you start vomitting within hours, if your food still has this enterotoxin in it when you ingested it (associated with the fried rice)
2) gastrointestinal toxin - delayed onset diarrhea - 8-16 hours later - is formed by the spores that germinate in the intestinal tract...this is the caterer's disease (associated with meats and veggies at catering events)
Describe the population at risk for lysteria infection?
1) Maternal listeriosis - Mothers may get a short, self resolving febrile state, but what can happen is this can transfer across the placenta to the fetus and cause an abortion (granulomatosis infantiseptica), or can be transferred and cause...
2) perinatal listeriosis - an early onset (within 5 days of birth) which leads to sepsis, and a later onset (after 5 days) which leads to meningitis
*Also, for very immunocompromised people listeria can cause sepsis and meningitis most frequently
Why are people with deficient cell mediated immunities at risk for listeria? ie people with HIV, T cell deficiency?
Because you need a T-cell mediated immune response and macrophages in order to kill of listeria (since its mainly intracellular)
How must you treat a listeria infection?
With antibiotics that CROSS the eukaryotic cell membrane since they are likely to be intracellular
Where is listeria?
Basically everywhere, its ubiquitos, especially because it can grow at 4 degrees C, we find it refrigerators, on our meats, hot dogs, cold cuts, unpasteurized milk and dairy products, soft cheeses...and yet it doesn't cause as much infection because most of us are not immunosuppressed, thus listeria attacks the immunosuppressed, neonates, and fetuses mainly
What are the two forms of transmission of diphteria and discuss the potential disease that may result...
1) Cutaneous - usually will not progress on to cardio or neuro disease
2) Respiratory - inhaled droplets, if goes untreated the toxin starts to disseminate into the circulation and this can cause myocardial and neural damage. Ultimately if untreated in this case, the person will die of cardio or neuro disease.
True or false - there are lots of carriers of diphtheria but whom are not producing toxin?
TRUE - the corynebacterium diphteria must be infected by the Corynebacterium beta phage which carries the gene for the toxin (dtx) before the strain can be considered TOXIGENIC
Discuss the environmental regulatory mechanism by when dtx is synthesized? And what is it like in the human environment?
In high iron conditions, the repressor protein is bound and activated by iron, thus dtx is NOT made. In low iron conditions, repressor protein is NOT bound by iron, therefore dtx is synthesized. In the body, we are in a low free iron state because transferrin and lactoferrin constantly suck up our iron.
Describe the hallmark of diphtheria infection and its components?
pseudomembrane - made up of fibrin, dead necrotic epithelium, bacteria, and neutrophils (lymphocytes...Hull also said mucous)
Discuss the three diagnostic tests one could use to determine diphterhias toxigenicity?
1) Shick Test - inject square parts of a rabbit with the supernatant and see what happens (if boils of puss or whatever appear)
2) PCR - this is becoming the mainstay due to ease and rapid results
3) Elek Immunodiffusion - streak your bacteria, and place perpendicular to them a strip soaked in anti-diphtheria toxin antibody. Strains that are toxigenic will form those wavy lines (precipitin lines) that look like a sin wave (because the toxin is interacting with its antibodies), those that are not toxigenic you will see no such waves for.
Why is 53% of the US susceptible to getting diphteria?
Because we are NOT getting our boosters! Every 10 years or so after our vaccination we are supposed to get boosters but we aren't (those who go to ERs for wounds or cuts will get a tetanus booster which also has the Diphtheria component but what about those ppl that don't get this?)
What are the 3 common forms of bacillus anthracis, and what is the most commonly presenting one in nature?
1) Respiratory, 2) Cutaneous, 3) Gastrointestinal....Cutaneous accounts for over 95% of the incidences (not talking about terrorism here)
Bacillus anthracis is found naturally in the soil, and since it sporulates its such a pester to kill them, but if ingested in grossly contaminated meat, what kind of symptoms would you see?
bloody diarrhea, nausea, vomiting, abdominal pain
Pulmonary inhalation of bacillus anthracis spores happens most commonly in people who...
work with animal hides, Woolsorter's disease, and with animal products too, guy who imported cow hides from africa to NY to make his drums...this form is usually fatal within 1-2 days
What is the name of the characteristic black center lesion that can form with cutaneous infection and is it painless or not?
Eschar, and yes it is painless
What are the two virulent factors carried on plasmids by bacillus anthracis?
1) its capsule
2) tripartate toxin
What is unique about the capsule of bacillus anthracis versus all other capsules?
It is NOT polysaccharide, it is made up of poly-D-glutamic acid (protein!)
Describe the mechanism of the bacillus anthracis tripartate toxin
1 binding, 2 activity regions. the binding region (PA...protective antigen) binds to its surface receptor on the cell where it is nicked, then a heptamer of these PAs form, now it can bind EF or LF (edema factor & lethal factor) which will then get into cell by endocytosis, then escape the endosome when its acidified and do their thing in the cytoplasm.
*Lethal factor - works on protein kinases (MAPKK) to kill the cell
*Edema factor - works on Calmodulin dependent adenylate cyclase to increase cAMP product and thus increase edema
There is a high correlation of what organism contaminating stir-fried rice because of the way it is made?
bacillus cereus
Bacillus cereus also makes an enzyme called _________ that damages ocular tissue and causes ___________
lecithinase, endophthalmitis